Veterinary Quarterly

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Spontaneous primary myopathies in domestic

mammals: A review

S. A. Goedegebuure

To cite this article: S. A. Goedegebuure (1987) Spontaneous primary myopathies in domestic

mammals: A review, Veterinary Quarterly, 9:2, 155-171, DOI: 10.1080/01652176.1987.9694092

To link to this article: https://doi.org/10.1080/01652176.1987.9694092

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REVIEW PAPERS

Spontaneous primary myopathies in domes-

tic mammals: a review
S. A. Goedegebuure'

SUMMARY By reviewing the literature concerning primary myopathies in man and

animals, a classification of spontaneous primary myopathies in domestic mammals is made.
This classification is based on aetiological factors.
Primary myopathies are divided into metabolic, immunologic, toxic, nutritional, congenital,
inherited, and inflammatory myopathies. Muscular dystrophies, in accordance with the
definition in human cases, are considered as a separate entity. In the description of the
different muscle disorders the emphasis is on the structural changes and the pathogenesis.
Clinical signs and diagnostic criteria are considered only briefly.

INTRODUCTION

In animals many generalised and local disorders of skeletal muscle are known to
occur. In the last fifteen years a large amount of information and knowledge
concerning this subject has become available in the veterinary literature. Some
muscle disorders, of considerable economic importance, have been the subject of
detailed studies. The development of specialised enzyme histochemical and bio-
chemical methods, together with ultrastructural investigations, has created a better
understanding of muscle cell changes. The use of electromyography and electro-
neurography has supported this knowledge.
Pathological changes in skeletal musculature can be induced by neurological
disorders (neuromuscular diseases) or are due to primary muscle disorders (myopa-
thies). The term primary myopathy is applied to any disorder which can be
attributed to primary morphological, biochemical or electrical changes occuring in
the muscle fibres or in the interstitial tissues of voluntary musculature, and in which
there is no evidence that such changes are in any way secondary to changed function
in the central or peripheral nervous system (101).
In this review only spontaneous primary myopathies in domestic mammals will be
considered. Disorders of the neuromuscular junction (motor end-plates) are in fact
neuromuscular diseases, but they are considered here together with the primary
myopathies. Changes in muscular tissue due to physical injuries or circulatory
disturbances are not included, nor are local disorders such as tumours or tumour-
like conditions.
In the description of the different muscle disorders the emphasis will be on the
structural changes and the pathogenesis. Clinical signs and diagnostic criteria will
be considered only briefly.

CLASSIFICATION

Classification of primary myopathies with regard to pathological changes only is

difficult if not impossible. Muscle cells suffering acute damage from different

Department of Veterinary Pathology, Statc University Utrecht, Yalelaan I, Postbox 80.158, 3508 TD
Utrecht, The Netherlands

THE VETERINARY QUARTERLY, Vol_ 9, No. 2, APRIL 1987 155

causes tend to go through common pathways of changes, because of the limited
repertoire of the muscle tissue in its reaction to injury. In chronic disease, even
obviously different changes in the primary stages may result in similar or identical
end stages.
The most useful basis for classification at present is aetiology, although this may be
unknown, poorly understood or complex. This classification is based on the earlier
work of Bradley and Fell (14) and Hul land (47) in animals, and Dubowitz (34),
Mastaglia (61), Sarnat (83), Schröder (84) and Walton (101) in man. The aetiologi-
cal factors are metabolic, nutritional, toxic, immunologic, hereditary and inflam-
matory. The spontaneous primary myopathies of domestic mammals are listed in
Table 1. However, there is a frequent overlap apparent in their aetiologies, and
therefore such a classification cannot be precise. Particularly the question of
Table I. Classification of spontaneous primary myopathies in domestic mammals with regard to
aetiological factors.

Metabolic myopathies Muscular dystrophies

Porcine stress syndrome Weaver syndrome of Brown Swiss cattle
Back-muscle necrosis in pigs Muscular dystrophy of MRY cattle
Azoturia-Tying up Muscular dystrophy of Merino sheep
Azoturia-like syndromes Pietrain creeper syndrome
Capture myopathy Muscular dystrophy in dogs
Transport myopathy Muscular dystrophy in cats
Postanaesthesia myopathy in horses Inflammatory myopathies
Myopathy associated with hyperadrenocorticism Blackleg
Myopathy associated with hypothyroidism Pseudoblackleg
Glycogen storage disease Gas gangrene and malignant oedema
Mitochondrial myopathy in dogs Suppurative myositis
Immunologic myopathies Changes secondary to systemic infections
Myasthenia gravis Changes secondary to non-infectious
Toxic myopathies systemic diseases
Phytotoxins Eosinophilic myositis in cattle and sheep
Chemical toxins Myositits of masticatory muscles in dogs
Nutritional myopathies Parasitic myositis
Nutritional myodegeneration Miscellaneous group of myopathies
Masticatory myositis in horses Muscular steatosis
Congenital and inherited myopathies Myotonia
Splay leg Xanthosis
Arthrogryposis congenita Canine pectineus muscle hypotrophy
Congenital myopathy in lambs Myopathy of cachectic sheep
Double-muscling
'Daft lamb' disease

heritability has been a problem. In some myopathies a proven heredity is present, in

others this is suspected by the occurrence of disease in only single breeds or families.
If besides a hereditary factor another aetiologic factor is known, e.g. metabolic or
immunologic, the myopathy is classified under that heading. As in man, a special
classification of muscular dystrophy is made. The myopathies in this group more or
less fulfil the criteria used in the human definition for muscular dystrophy. A
separately classification of congenital myopathies is made, including a group with
proven inheritance, and a group with suspected or no inheritance.
With further progression in knowledge, it is likely that some of the separate entities
described will be found to have common factors, and will coalesce. In man, there
are strong indications that some muscular dystrophies have primary enzyme defi-
ciencies which are responsible for the pathogenesis. Until now, such findings are
lacking in domestic mammals, but when present and proven, such muscular dys-
trophies can be considered as real metabolic myopathies. The same applies to some
inflammatory myopathies, i.e. if the underlying suspected immunologic basis can
be proven, they must also be so classified.

156 THE VETERINARY QUARTERLY. VOL. 9, No 2, APRIL 1987

Some authors consider the exertional myopathies, such as porcine stress syndrome,
azoturia and tying up, capture and transport myopathy, as a separate group. In this
review they are classified under the metabolic myopathies, because abnormal
glycogen metabolism is the primary change.

MAIN PATHOLOGICAL CHARACTERISTICS OF SPONTANEOUS PRIMARY MYOPA-

THIES IN DOMESTIC MAMMALS

Metabolic myopathies
This is a group of diseases related only by the common theme of the molecular basis
of myopathic processes, in which a metabolic or endocrinological aetiologyis more
or less specifically known; such diseases are well known in farm and pet animals.
Porcine stress syndrome (PSS) affects malignant hyperthermia-susceptible swine
under stress conditions (excitement, fighting, transportation), and often may result
in sudden death. Stress susceptibility is related to an increase in the mass of muscles
which in term is associated with a.. increase in the proportion of type II fibres.
Muscles with a normally high proportion of type II fibres, such as longissimus,
psoas and semitendinosus, are therefore most extensively and most frequently
affected. Affected muscles appear pale, soft and exudative (PSE). Oedema between
muscle fibres, contraction bands and floccular desintegration of the fibres are the
most characteristic histological findings in affected muscles. In cases of prolonged
but non-fatal stress, muscles appear dark, firm and dry (DFD), and have poor
keeping qualities. Myocardial lesions include multifocal granular degeneration,
contraction band necrosis, and myocytolysis.
The common denominator in the biochemical changes in PSE seems to be an efflux
of mitochondrial Ca++ within the muscle fibres, resulting in an increase in myofibril-
lar ATPase and phosphorylase kinase, leading to rapid glycolysis. This rapidly
raises body heat and lactate and lactic acid levels producing local and generalised
acidosis. PSS is influenced by heritable factors (23,36,52,90).
Back-muscle necrosis in pigs. This is a particular manifestation of the porcine
stress syndrome. Gross lesions consistently appear in longissimus muscle. In the
acute form haemorrhages and large foci of necrosis are present, in chronic cases
atrophy and fibrosis are predominant. Histological features are non-specific: hya-
line degeneration and necrosis of muscle cells, phagocytosis, cellular infiltration
and fibrosis (8,17).
Azoturia (paralytic myoglobinuria, Monday morning disease) and Tying up (set-
fast, acute rhabdomyolysis). Azoturia is a severe, and frequently fatal acute
myodegeneration in mainly working horses, while tying up is the milder form of the
disease in riding and racing horses.
Azoturia typically occurs very shortly after beginning work or training following
some days of rest on full working rations. Muscular lesions are often widespread,
but changes in gluteal, lumbar and quadriceps muscles are most obvious. Muscles
are swollen, moist, and dark with streaks of pallor.
Histologically, the initial lesions are in type II fibres, and are characterised by
hyaline changes in segments of fibres. In more severe cases hyaline and floccular
changes with phagocytic inflammatory cells are widespread in all fibres. Within a
few days, regenerative repair restores muscle fibres. Degenerative myocardial
lesions may occur. Renal complications by myoglobin lead to renal failure and
death.
Tying up sometimes follows a period of rest, but is mostly an acute recurrent disease
following increased exercise. Lumbar and gluteal muscles are usually the sites of

THE VETERINARY QUARTERLY. vol . 9, No. 2, APRIL 1987 157

 most severe lesions. Grossly visible changes are not present. Dependent on the
severity, 0.2-5% of muscle fibres in a biopsy sample may be affected. Degenerated
fibres are solitary, predominantly in type II fibres, and contain hyaline and floccu-
lar segments. Affected animals and muscles recover rapidly and completely.
It is postulated that in both azoturia and tying up intensive or exhaustive activity of
muscles is associated with rapid or aberrant utilisation of glycocen and that this
turnoff generates local heat and lactic acid. These two products, concentrated
locally in type II fibres, modify contractile proteins of muscle fibres and result in
degenerative changes. Diffusion of lactic acid and heat leads to degenerative
changes in adjacent fibres of all types (47,59,65).
Azoturia-like syndromes are known occasionally in other species. Muscle degener-
ation and myoglobinuria are described in cattle, sheep and racing greyhounds
following exercise (2,9,77).
Capture myopathy. This acute myopathy is often associated with acute death, and
occurs in sheep and many wild animals after exhaustion by chase, struggle, etc. Pro-
found acidosis is often associated with capture myopathy. Morphological lesions
and pathogenesis are similar to those in azoturia (7,44).
Transport myopathy. Especially in cattle, and sometimes in horses and sheep, a
muscle disease closely resembling nutritional myodegeneration occurs after physi-
cal activity or transport. Energy depletion at the intracellular level rather than
membrane alteration seems to be the primary cause in this type of myodegeneration
(14,29,95).
Post anaesthesia myopathy in horses. This syndrome can be identified clinically in
two forms. The first is a local myopathy, and triceps muscles or the extensors of the
hindlimb or the gluteal muscles may be involved. The second is the generalised
form, in which both pectoral and pelvic girdle muscles are affected. Muscular
lesions are the same in both forms, and are similar to acute rhabdomyolysis.
Histochemical examination shows initial degeneration and necrosis of type II
muscle cells.
Increase in intracompartmental pressure whith subsequent ischaemia appear to be
the causal aetiology in the local form, while in the more generalised form also stress,
excessive use of muscle relaxants or muscle sensitivity to anaesthetics are involved.
Mitochondrial and myofibrillar calcium overload resulting in calcium release and
lack of energy produce hypercontraction and damage of muscle fibres (108).
Myopathy associated with hyperadrenocorticism. In adult dogs with longstanding
naturally mailing and iatrogenic hyperadrenocorticism a glucocorticoid-related
myopathy occurs. Both in cases with clinical symptoms (muscle weakness, atrophy
and stiffness, especially in the hindlimbs) and subclinical cases, myotonic dis-
charges are present on electromyography. Muscle biopsies reveal mild degenerative
changes of fibre size variation, focal necrosis with phagocytosis, fibre splitting,
internal nuclei and fatty infiltration of cells. Atrophy of type I and type II fibres
with type grouping is obvious. Endomysial and perimysial fibrosis and fat is
increased. Mitochondrial changes are the most prominent ultrastructural feature.
These myopathic alterations in hyperadrenocorticism may result from decreased
synthesis and increased catabolism of essential muscle proteins (20, 33, 38, 46).
Myopathy associated with hypothyroidism. In dogs with primary hypothyroidism
but without clinical neuromuscular disease myopathic changes are described. The
most prominent change is variation in fibre size, associated with atrophic type II
fibres and some hypertrophic type I fibres. There is also loss of type II fibres.
Myodegeneration and cellular response is not present. A disturbance of carbohy-
drate metabolism has been suggested to explain the preferential type II fibre
atrophy because of the greater dependance of type II fibres on glycogenolysis and
glycolysis for their energy supplies (19). .,

158 THE VETERINARY QUARTERLY, VOL. 9, No. 2, APRIL 1987

Glycogen storage disease (GSD). Inborn errors of glycogen metabolism have been
recognised in animals in relation to muscle disorders. However, in all cases it has
been part of a wider involvement of tissues.
In man eight types of inherited GSD have been clearly identified, each one being
associated with a particular enzyme deficiency. Only type II and III are docu-
mented with certainty in domestic mammals as spontaneous diseases.
GSD II (acid a-glucosidase deficiency) has been described in cattle and dogs. The
bovine cases occur in Brahman and Shorthorn cattle. The incidence is compatible
with autosomal recessive inheritance. Clinical signs are progressive muscle weak-
ness and inability to rise properly. Canine cases are in Lapland dogs, in which the
autosomal recessive inheritance has been confirmed by biochemical and genetic
investigation. Clinical signs are progressive muscle weakness and severe vomiting,
resulting in exhaustion and death at an age of 10-18 months. In both cattle and dogs
generalised glycogen storage is present, particularly involving the muscular tissues
including myocardial tissue. On light microscopy there is a marked vacuolar
myopathy. PAS-positive material and abundant acid phophatase activity can be
demonstrated in these vacuoles by enzyme histochemistry. Ultrastructurally the
presence of glycogen-containing membrane-bound vacuoles (glycogenosomes) by
regular cellular autophagy is obvious. Heterozygote detection is possible by bio-
chemical investigations in peripheral blood leucocytes.
GSD III (debrancher enzyme deficiency) occurs in German Shepherd dogs as a
possible autosomal recessive trait. Clinical signs, course and pathomorphologic
lesions are similar to GSD II.
Glycogenosis unspecified as to enzyme deficiency is recorded in horses, Corriedale
sheep, toy breed puppies and cats. Only on clinicopathological grounds were these
conditions comparable with GSD (6,60,73,79,102,103). .

Mitochondrial myopathy in dogs. A myopathy caused by abnormal mitochondral

function has been described in a litter of Irish terrier pups. Progressive clinical signs
are stiffness and muscle atrophy. Affected muscles are pale, with yellowish-white
streaks. Histology reveals patchy myodegeneration with phagocytosis and calcifi-
cation. Electron microscopy shows abnormal bizarre mitochondria. Biochemically
the mitochondria have normal oxidative phosphorylation but lack respiratory
control (loosely coupled mitochondria). The condition has a possible recessive
X-linked inheritance (106, 107).
Immunologic myopathies
A well-known proven example is myasthenia gravis. In the case of some other
myopathies, e.g. eosinophilic myositis of cattle and sheep, and myositis of the
masticatory muscles of dogs, an immunological basis is suspected only. For that
reason they will be considered elsewhere in this review.
Myasthenia gravis. This disease has been recognised rarely in dogs and cats.
Clinical manifestations are progressive stiffness, fatigue, vomiting and reduced
tolerance to exercise. Histologic changes in muscles are non-specific and sporadic
with atrophic changes, isolated foci of lymphocytes and fibrosis. There is reduction
in the number of acetylcholine receptors on the post synaptic membranes.
In animals with delayed onset of the disease, there appears to be defective function
of the thymus, leading to circulating auto-antibodies against acetylcholine recep-
tors. There is a link between the disease and thymic tumours. Animals with the
congenital form of myasthenia gravis show a recessive mode of inheritance for
depletion of acetylcholine receptors without an auto-immune basis (26,50,58,74,99).
Toxic myopathies
Only few phytotoxins and chemical toxins have been shown to cause naturally
occurring primary myopathies in domestic animals. In some cases there is a
THE VETERINARY QUARTERLY, Vol 9, No 2, APRIL 1987 159
 concurrent effect of nerve damage with symptoms of neuromuscular disease.
Toxins producing damage of only the nervous system are not considered here.
Phytotoxins. In the southern United States indigenous plants, the senna (Cassia
occidentalis) eaten by cattle and goats, and cotton seeds (containing the polyphyno-
lia substance gossypol) eaten by swine give rise to severe acute myodegeneration,
including myocardial lesions. Morphological lesions resemble those of nutritional
myopathy. In Australia a lupinosis-associated myopathy in sheep and a myopathy
in sheep fed grain and/or cereal roughage is known to occur. In the latter a calcium
deficient state has been suggested as an aetiological factor. Pathological lesions are
similar as in nutritional and exertional myopathies (1,42,67,76).
Monensin, an ionophorous antibiotic derived from Streptomyces cinnamonensis,
is used as a coccidiostat in poultry, and a feed additive for cattle, in which it
increases feed use by altering rumen fermentation. Toxicosis has been reported in
equidae, sheep, cattle, pigs and dogs. Macroscopic and histologic lesions differ very
little from those of nutritional myopathy. Hindlimb muscles are involved most
severely and myocardial lesions occur. Swelling and disintegration of mitochondria
are the first visible lesions, caused by the interference of monensin with normal
sodium and calcium cellular membrane transport. This interference leads to mito-
chondrial calcium overload and muscle cell necrosis (3,24,68,78,111).
The myodegeneration in sheep eating toxic plants (Solanum esuriale) in Australia
is not a primary myopathy (as thought for a long time), but is a form of transport
myopathy superimposed on primary innervation loss by the plant toxins (72).
Chemical toxins. Selenium, iron, thallium, and perhaps sulphur and cobalt, when
fed at appropriate levels, have caused natural muscle diseases in domestic animals.
The intermediate stages seem in all cases to be related to the mechanisms associated
with nutritional myopathy, and lesions in skeletal and cardiac muscles are therefore
similar to that myopathy (14,47,87,96).

Nutritional myopathies

Deficiencies are principally responsible for these myopathies. They occur all over
the world in all domestic mammals. The disease is a primary myodegeneration and
not a muscular dystrophy.
Nutritional myodegeneration (white muscle disease, stiff-lamb disease, nutritional
muscular dystrophy). This is caused by deficiency of selenium and or vitamin E
(a-tocopherol); toxicants and environmental factors may contribute to this disease.
Pigs, cattle and sheep are most susceptible, horses and goats are moderately suscep-
tible, while occasional cases in dogs and cats have been described. The disease occurs
predominantly in young animals, but both congenital forms, and occurrence in
mature and old animals have been reported.
Clinical signs are variable and dependent on the severity and muscles involved;
shuffling gait, stiffness, tremor and dyspnea are obvious in severe cases, acute death
occurs in cardiomyopathy. Myoglobinuria is seen in only older animals. Mortality
is variable, but may reach 50%. The larger muscles of the shoulder and thigh are
predominantly involved, but back, neck, respiratory and cardiac muscles may be
also affected. Involvement is nearly always bilateral. Affected muscles are pale,
irregularly opaque, with white brush strokes from calcification. Histological
lesions are characterised by hypercontraction, hyaline, floccular and granular
degeneration and fragmentation of muscle fibres, with or without abundant calcifi-
cation and phagocytosis. The ensheathing structures and satellite cells remain
intact, thereby enabling a rapid and efficient regenerative repair, with only slight
fibrosis. Myocardial lesions are mostly not repaired by muscle cell regeneration but
by replacement with condensed stroma. Histochemical examination reveals a

160 THE VETERINARY QUARTERLY, VOL 9, No. 2, APRIL 1987

preferential but not exclusive type I fibre degeneration. The earliest detectable
change by electron microscopy is degeneration of mitochondria, followed by loss of
some parts of the sarcomeres and disintegration of the tubular systems.
Subcellular changes are the basic result of dietary deficiency of selenium or vitamin
E (a-tocopherol). Although the metabolism of Se and vitamin E is incompletely
understood, in general the following pathogenesis might be considered. Both
vitamin E and selenium-containing enzymes (the glutathione peroxidase-glutathi-
one reductase system) are required in muscle cells and many other cells, as physio-
logic antagonists to free radicals (products of normal cell function). Absence of
sufficient protection against free radicals leads to modification of cellular mem-
branes and cellular injury by causing peroxidation of membrane lipids and physico-
chemical damage to protein molecules, including those of mitochondria, endo-
plasmic reticulum and cytosol. This initiates the sequence of mitochondrial calcium
overload (by change in membrane gradients) and depletion of the energy system,
which leads to calcium-induced hypercontraction of myofibrils and degeneration
of myofibres.
Climate-related conditions, dietary metallic toxicants, duration of storage of the
fodder, copper deficiency in the dam, sulphur fertilisers for pasture, physical
activity, injection of iron-containing products in pigs, and excessive intake of
polyunsaturated fats are known triggering factors for nutritional myodegenera-
tion. The syndrome of nutritional myopathy is aetiologically complex
(14,27,47,81,82,93,112).
Masticatory myositis in horses. In foals and sometimes in poorly nourished stable
horses, a myopathy of the masticatory and tongue muscles occurs; some animals
develop steatitis concurrently. On clinical and pathologic grounds this syndrome
seems to be part of nutritional myodegeneration as described above. However,
detailed studies are lacking (55).

Congenital and inherited myopathies

Congenital myopathies are common in all kinds of domestic animals and are ,

sometimes of economic importance, but detailed morphological descriptive find-

ings are lacking or quite superficial in many cases. Some are proven to be inherited,
others are claimed or suspected to be so, and others are known to be not inherited.
Inherited defects may be congenital or of early or delayed postnatal onset.
A lot of these myopathies have a primary defect in the neural system or primary
defects in both the neural and muscular systems. Only myopathies with a primary
defect in the muscular system are considered in this review.
Splayleg (spraddle leg, myofibrillar hypoplasia). This is an economically import-
ant, transient disease of neonatal piglets in all countries with intensive pig rearing.
The incidence may be high, e.g. in Britain 0.4 percent or 60,000 piglets per year, with
a mortality rate of about fifty percent (caused by starvation, accidents, etc.). Piglets
which survive recover spontaneously within a week. Frequently the occurence is a
farm or regional outbreak. The incidence in litters is variable. The muscles chiefly
affected are the longissimus, semitendinosus and triceps.
Macroscopically subcutaneous and interstitial oedema may be visible in the hind-
limbs. On light microscopy a lightness of staining with eosin and variable myofi-
brillar hypoplasia is obvious. Electron microscopically, a series of degenerative and
hypoplastic changes occur segmentally in the muscle fibres. These findings are
however not pathognomonic of splayleg. The same changes may be present,
although less commonly and less obviously, in normal litter mates.
The aetiology and pathogenesis are still not understood. The aetiology is probably
polygenetic and multifactorial. A dominant sex-linked hereditary factor with

THE VETERINARY QUARTERLY, VOL 9, No. 2, APRIL 1987 161

 incomplete penetrance, trauma, defective maternal nutrition, ingestion of fungal
toxins in the food of the pregnant sow, may play a role. Dysmaturity of skeletal
musculature seems to be one of the most important pathogenetic factors. Irregular-
ity or retardation in the transition of type II fibres into type I fibres in the late
intrauterine and early postnatal period is the hallmark of this dysmaturity. This
retardation is corrected at about 7 days posnatally (25,92,104).
Developmental abnormalities of spinal closure and myopathy induced by the injec-
tion of saccharated iron may produce a similar clinical syndrome in piglets, but
without myofibrillar hypoplasia (30,75).
Myofibrillar hypoplasia has been reported in a 6 week old calf, with the same
characteristics as in Splayleg piglets, but also with absence of Z-discs, sarcoplasmic
inclusions and nuclear abnormalities (12).
Arthrogryposis congenita. This is a common disease of calves, lambs, foals and
piglets, and less frequently of kittens and puppies. The disorder is characterised by a
congenital dysfunction of one or more joints. In the majority of cases the primary
defect may be in the nervous system, but sometimes the primary defect may be in
the muscular system. In the latter the muscles show degenerative changes and/or
hypotrophy, and an increase of adipose and fibrous tissue. However, such changes
may also be secondary. Genetical and environmental factors are held responsible
for these primary myopathic lesions (14).
Congenital myopathy in lambs. Myodegeneration with calcification, muscle cell
atrophy, fibrosis and muscle cell regeneration are described in Suffolk lambs in
Scotland with congenital abnormalities of the muscular system. Exact causes have
not been found, but it was suggested that deficiency of vitamin E or selenium
(nutritional myopathy) might be responsible for this syndrome. It is thus debatable
if it should be considered to be an exclusive syndrome (69).
Double-muscling (hyperplasia of muscle fibres). This anomaly of muscles is of
economic importance in many breeds of cattle. Some or all of the muscles may be
hypertrophied, and upper hindlimb muscles are always involved. Microscopically
there is muscle cell hyperplasia, with a decreased number of type I fibres, and an
increased number of hypertrophied type II fibres. The latter makes these animals
more susceptible to stress. The condition is inherited as an autosomal recessive
trait, with a variable expression in the heterozygous animal. The condition has been
reported occasionally in sheep (10).
'Daft lamb' disease. This disease occurs only in Border Leicester sheep in England,
and is inherited as an autosomal recessive trait. Lambs born are unable to rise, or
develop a stiff gait within a few days. A 'star-gazing' position of the head is always
present. Affected muscles, particularly the neck muscles, show abnormal variation
in muscle cell size by abnormal enlargement of some type I fibres and smaller size of
all other fibres. It is not clear whether there is a primary defect in the muscle cells,
either alone or together with a neuropathy (11,15,91).

MUSCULAR DYSTROPHY

In man a muscular dystrophy is adequately defined as a group of progressive,

genetically determined, primary degenerative myopathies. They are usually not
present at birth, and the neural and vascular components of muscle are not initially
involved. Regeneration of muscle cells is absent or inadequate. On genetic, clinical
and pathological grounds the dystrophies are subdivided into various groups, as
Duchenne type, limb-girdle type, etc. (34,61,84,100).
In the past, several animal (neuro)muscular lesions were referred to as muscular
dystrophy. The current human definition is used by most authors to classify several
animal myopathies as dystrophies. For that reason such lesions are more clearly

162 THE VETERINARY QUARTERLY, VOL. 9, No. 2, APRIL 1987

defined and therefore diminished in number. However, in animals descriptions of
real muscular dystrophies are infrequent and often inadequate; a proven genetic
basis is usually lacking. For that reason muscular dystrophies and suspected
dystrophies (dystrophy-like myopathies) are summarised here together.
Weaver syndrome of Brown Swiss cattle. The disease develops at an age of 6
months. The gait of the hind limbs becomes abnormal and erratic until the animals
are permanently recumbent. Lesions are present in the muscles of only the loin and
hindquarters, which show hyaline and vacuolar degeneration, splitting and frag-
mentation of muscle fibres, and proliferation of connective tissue. A possible
inheritance is presumed (52).
Muscular dystrophy of Meuse-Rhine-Yssel cattle. This condition occurs in a small
area of the eastern part of The Netherlands. Some 100 cases have been documented,
all females, aged from 2 to 10 years. The disease is progressive, with clinical signs of
loss of appetite, diminished rumination, less frequent eructation, recurrent bloat,
and dyspnoea which leads finally to asphyxia. Electromyographically only the
diaphragmatic muscles show aberrations. Macroscopic lesions are found in only
the muscular part of the diaphragm, which is diffusely pale, swollen and unpliable.
Histologically, the diaphragmatic muscles always show severe and extensive
lesions, characterised by variation in size of muscle fibres, vacuolar and hyaline
degeneration with fragmentation and phagocytosis, increase of internal nuclei,
fibre splitting, absence of regeneration, and proliferation of endomysial and peri-
mysial connective tissue. Core-like structures are usually predominantly present.
Both fibre types are involved. The intercostal muscles in all cows have core-like
structures and variable degenerative changes; lesions are always less severe than in
the diaphragmatic muscle. Other skeletal muscles may or may not have a variable
number of core-like structures. Hereditary transmission is not proven, but a strong
familial relationship is present. Sub-clinical cases (carriers) are present (37,45).
Muscular dystrophy of Merino sheep. In particular flocks of lambs of the Merino
breed in Australia a progressive myopathy occurs in 1-2% of the progeny each year
after they reach 1-4 months of age. There is no sex prevalence. Lambs show
decreased growth and flexion of the hind limbs, which leads to stiffness and gait
aberrations. Progression of the disease results in death from starvation at 6 to 18
months of age. Macroscopic lesions are always present in the vastus intermedius
and quadriceps femoris: white areas or totally white muscles. Histologically the first
lesions in these muscles are rounding of the muscle cells in cross-sections, with
variation in size, the appearance of central and peripheral sarcoplasmic masses,
increase of internal nuclei and slight vacuolar degeneration with phagocytosis. As
the lambs age there is reduction in the number of muscle cells, which are progres-
sively replaced by fat cells. In other muscles similar changes are present to a much
lesser degree. Inheritance with a recessive autosomal trait has been proposed, but is
not proven (28,62,63).
Pietrain creeper syndrome. In a pure bred Pietrain herd in England a progressive
muscular tremor is observed. The onset is at 2-3 weeks of age, resulting in a creeping
type of gait and recumbency. Proximal limb muscles are most affected and micro-
scopically show severe atrophy. Microscopically all major muscles appear to be
affected with wide variation in muscle cell size, increase in internal nuclei, and focal
myodegeneration. Both type I and type II fibres are involved with a change in the
distribution pattern of the types. The condition is familial and possibly inherited
(16,105).
Muscular dystrophy in dogs. Reports on muscular dystrophy in dogs are rare.
Isolated cases of dystrophy-like conditions are usually described. The disease
affects young and adult dogs of either sex and different breeds. Muscle weakness is
the predominant clinical sign in all cases; histopathological features are variable,

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but variation in fibre size, focal myodegeneration, cell splitting and replacement by
fat tissue is consistent. Regeneration is nearly always absent (47,51,66,109).
A well-documented primary myopathy in Labrador retrievers has been reported in
the United States and in the United Kingdom. This condition is transmitted by a
simple autosomal recessive mode. Affected animals show clinical signs as early as 3
tot 4 months of age: stiff, stilted gait with short, mincing limb movements, pelvic
limb hopping and generalised muscle atrophy. These signs tend to stabilise in
animals older than 6 to 12 months of age. Muscle pathology consists of dissem-
inated fibre atrophy and multifocal presence of giant fibres, together with necrosis,
increased internal nuclei, fibre splitting and progressive fibrosis. There is apparent
type II fibre depletion on enzyme histochemistry. The condition is thought to be a
primary degenerative disorder, but a possible neurogenic role cannot be excluded
(18,35,53,54,64).
Recently a progressive muscular dystrophy, with a probable sex-linked inheritance,
has been described in young male Golden Retriever dogs. There is early onset of
generalised muscle weakness, stiff gait, and marked elevation of serum creatine
kinase. Morphologically there is marked hypercontraction and segmental necrosis
of muscle fibres with phagocytosis and regeneration (94).
Muscular dystrophy in cats. Only two reports concerning dystrophy-like condi-
tions in cats are available. The first describes a familial dystrophy-like myopathy in
a litter of Siamese kittens, the other a similar condition in a litter of European
shorthair tomcats. In both cases lesions were generalised in the skeletal muscula-
ture with the same features as in the isolated cases in dogs (47,98).

INFLAMMATORY MYOPATHIES

Many infectious agents (bacteria, viruses, parasites) are frequently the cause of an
inflammatory or degenerative response of muscle tissue. Some of them give more or
less the classical primary inflammatory reaction of the vascular connective tissue
(=myositis). Others give rise to only (often mild) degenerative reactions of muscle
cells (=myopathy). On the other hand an inflammatory reaction induces second-
ary degenerative changes, while primary degenerative changes activate an
inflammatory reaction. Therefore, especially in subacute to chronic cases, a clear
distinction between the two is often not possible. In many cases the cause of a
myositis is evident, in some others the aetiology is more complex or unknown.
Blackleg (emphysematous gangrene). This is a gangrenous myositis of ruminants
caused by Clostridium chauvoei and characterised by the activation of latent spores
in muscle. The disease has a rapid clinical course, animals are often found dead.
Affected muscles are usually the large muscles of the pectoral and pelvic girdles, but
lesions may be found in any striated muscle, including the myocardium. Macro-
scopically the affected areas are red-black, dry, friable, and gasfilled, with an odour
like rancid butter. The surrounding subcutaneous tissues and fascia are thickened by
a yellow, gelatineous fluid. Microscopically a severe cellulitis with copious oedema
and haemorrhage is evident. Degeneration and necrosis of the muscle fibres is
caused by both diffusing toxins and injury to blood vessels. Exudate and gas
bubbles separate bundles of fibres and individual fibres.
The infection is acquired by the ingestion of spores, after some germinative cycles in
the gut, and their distribution to tissues where they may be stored for long periods
in phagocytic cells!' Local events creating muscle damage or low oxygen tension
stimulate these latent spores to germinate (47).
Pseudoblackleg. This myositis occurs in ruminants, mimics blackleg very closely,
but is caused by Clostridium septicum. Detectable wounds are not present. Muscle
lesions have the same character as in blackleg, but are less extensive (47).

164 THE VETERINARY QUARTERLY, VOL. 9, No. 2, APRIL 1987

Gas gangrene and malignant oedema. These conditions are essentially wound
infections in which Clostridium septicum, C. perfringens, C. novyi, C. sordelli and
C. chauvoei are the principal pathogens. Ruminants, horses and swine are highly
susceptible. Germination of spores and vegetative growth occur in precise local
anaerobic conditions in deep penetrating wounds, as may be seen after castration,
shearing, injuries during parturition, stake wounds, etc. In gas gangrene there is
extensive disintegration of muscle with saturation of the tissues with serous or
sanguineous exudate and bubbles of gas, while in malignant oedema especially the
connective tissue is involved by extensive oedema and cellulitis, with sparing of the
muscle fibres. In both cases animals can die rapidly from systemic intoxication. A
typical wound infection by Clostridium novyi in rams is the so-called 'swollen head'.
Caused by fighting, and usually fatal within 48 hours (47).
Suppurative myositis. Abscesses in muscles may be haematogenous in origin, or are
the result of penetrating wounds and inoculations or of extension of a focus in
adjacent structures. Corynebacterium pyogenes in cattle, C. pseudotuberculosis in
sheep and goats, and Streptococcus equi in horses are the most frequent causative
agents. In all species a variety of staphylococci and streptococci may be also
responsible. Depending on the stage, ill-defined cellulitis with necrotic muscle
fibres or well-organised abscesses are possible. In early cases a local cellulitis can
give rise to a rapidly expanding cellulitis of muscle and adjacent structures (phleg-
monous inflammation) (47).
Changes secondary to systemic infections. In many acute systemic infections both
bacterial and viral, degenerative changes of muscle fibres occur in all species. The
lesions are widespread, not recognisable grossly, and consist of segmental degener-
ation of a few or many fibres with retraction of fibre segments. Phagocytosis is
sparse. Survival of the animal from the systemic infection should allow complete
restoration of the muscle damage (47).
Changes secondary to non-infectious systemic diseases. Polymyositis in dogs has
been reported in association with cases of systemic lupus erythematosus and cases
of systemic malignancies. Progressive muscular weakness is the principal clinical
sign. Histologically there are perivascular infiltrations of macrophages, plasma
cells and lymphocytes widespread in the muscles, beneath a slight myodegenera-
tion, phagocytosis, fibre atrophy and some regeneration (40,56).
Eosinophilic myositis of cattle and sheep. This is a rare myositis in cattle and sheep
of all ages, and its main significance is in meat inspection. However, fatal cases from
myocardial involvement have been reported. Lesions may occur in single muscles,
or groups of muscles, or even more widespread. Their size varies from some
millimetres to 10 cm in diameter, being well-demarcated, brown-green to grey-
green in colour, and pronounced on the surface. Histologically, the reaction is
characterised by large numbers of eosinophils in the endo- and perimysium while
degeneration of muscle fibres is slight. Later, fibroplasia and loss of muscle fibres
are evident, many eosinophils are still present, together with lymphocytes, plasma
cells, and histiocytes. The aetiology of this condition is obscure. Formerly Sarco-
cystis was often suspected. It is now suggested that an allergic reaction focused on
muscle is responsible. A heat-stable, eosinophil-chemotactic substance has been
isolated from affected bovine muscle. Its activity seems to correlate with lesion size
and severity (43,47,70,89).
Myositis of masticatory muscles in dogs. Myositis of temporal, masseter and
pterygoid muscles have been reported in dogs as eosinophilic myositis and atrophic
myositis.
Eosinophilic myositis occurs most often in German Shepherds of all ages, and is
characterised by recurrent attacks of pain, mandibular immobility and swelling of
the masticatory muscles. During the acute phase, a moderate leucocytosis, with 10

THE VETERINARY QUARTERLY. VOL. 9, No. 2, APRIL 1987 165

 to 40% eosinophils, is present. Lesions are bilaterally symmetrical. The disease is
progressive and muscular atrophy gradually becomes obvious. In acute lesions
numerous eosinophils and smaller amounts of lymphocytes, plasma cells and
neutrophils are present, beneath focal and spreading areas of muscle degeneration
and necrosis. In the more chronic stages plasma cells predominate with extensive
muscle atrophy, progressive fibrosis and scant regeneration of muscle fibres.
Atrophic myositis occurs in various dog breeds of all ages, and has a mild,often
undetectable, acute onset. The course is chronic and progressive. Eosinophilia is
absent. Histological lesions are similar as in chronic cases of eosinophilic myositis:
severe atrophy and destruction of muscle fibres, a large amount of plasma cells and
lymphocytes and extensive fibrosis.
In both syndromes, cases occur with involvement of muscles other than the mastica-
tory muscles, and a real polymyositis is present. In spite of some differences in
clinical and pathological features it is now believed that both syndromes may be
basically one disease with varied expressions. The cause is unknown, but the
characters of the tissue reaction could be consistent with immune mediation.
Demonstration of immunoglobulins and anti-skeletal muscle antibodies have thus
far failed, however (5,40,47,71,85,110).
Parasitic myositis. Tissue cysts of the protozoan parasite Toxoplasma gondii may
sometimes produce, with a heavy infestation, a polymyositis in young pups and
kittens. Inflammatory reaction with granulocytes, lymphocytes, histiocytes and
plasma cells, together with segmental degeneration and regeneration of muscle
fibres, may be widespread in several muscles, including cardiac muscles (47).
Fourteen species of the protozoal parasite Sarcocystis are regularly found in muscles
of cattle, sheep, goats, horses and swine, as part of the intermediate host infection.
Particularly the schizogonous phase may cause severe clinical disease and death by
extensive fibre degeneration and marked enzyme release in heavy infestations.
Mature parasitic cysts, lying in the muscle cells, are rarely accompanied by inflam-
matory cells. Degenerated cysts are surrounded by a variable amount of inflamma-
tory cells and granulation tissue, showing small white, well-circumscribed lesions
on macroscopical inspection (47).
The larval form (cysticercus) of 3 tapeworms of carnivores have a special predilec-
tion for skeletal muscle in domestic mammals: Cysticercus cellulosae in pigs, Cysti-
cercus bovis in cattle and Cysticercus ovis in sheep and goats. Heart and mastica-
tory muscles are involved preferentially, although cysts may be often widespread
throughout the muscles. Cysts are easily visible macroscopically: 1-2 cm in diame-
ter, with a single inverted scolex, between muscle fibres. Histologically the cystsare
ensheated with dense connective tissue capsule and surrounded by some eosino-
phils and lymphocytes. This reaction may be abundant in degenerated cysts.
Encysted larvae of the nematode Trichinella spiralis are found in the muscle cells of
pigs, horses, dogs and cats. The larvae lie in a bulging glassy segment of muscle fibre.
There is usually one per fibre, up to 100 pm long. They are loosely encircled by
eosinophils and by a scattering of lymphocytes, macrophages and plasma cells.
When parasitised muscle segments degenerate, there may be a larger area of acute
inflammation, with eosinophils predominating. Larvae may survive more than 20
years (47).

MISCELLANEOUS GROUP OF MYOPATHIES

Some myopathies of unknown aetiology and which cannot be classified by sus-

pected aetiology under one of the other headings, are summarised.
Muscular steatosis (pseudohypertrofia lipomatosa). The condition is relatively
rare, and occurs in cattle and pigs. There are no clinical signs, and it is usually a

166 THE VETERINARY QUARTERLY, VOL. 9, No 2, APRIL 1987

problem only in meat inspection. Often it affects only one or several muscles of the
neck, back or upper limbs. The extent of lesions within a muscle can vary consider-
ably. Microscopically there is hyperplasia of fat cells and atrophy of muscle cells,
without evidence of inflammatory, degenerative or regenerative changes. The cause
is unknown, although congenital vascular hypoplasia is suggested. The condition
must be differentiated from the chronic course of several muscle diseases (41).
Myotonia (muscular tetany). This disorder is defined as 'continued active contrac-
tion of a muscle which persists after the cessation of voluntary effort or stimula-
tion'. Electromyography shows high-frequency discharges and 'dive bomber'
sounds as a consistent hallmark. The condition is rare in sheep, goats and dogs, and
extremely rare in calves and foals. The disease is probably inherited in goats and at
least familial in Chow Chow dogs and Shropshire lambs. Clinical signs develop at a
young age, and become increasingly severe with age. Affected animals become rigid,
have shifting lameness, and may be unable to move for several seconds.
Histological lesions are absent in routine sections in goats. Histochemical stains
reveal increased PAS-positive material and increased mitochondrial calcium
within fibres. Ultrastructural increased density of transverse tubules, proliferation
of sarcotubular elements and abnormal mitochondria are present. In lambs only
muscle cell hypertrophy and hyperplasia, and some myodegeneration is seen. In
dogs increase in size and rounding of muscle cells in cross-section, and numerous
internal nuclei are present, beneath some myodegenerative features and fibrosis.
The primary defect is considered to lie in the sarcolemma of the muscle cell, which
has increased resting membrane resistance due to low chloride conductance. The
product of increased resting membrane resistance is an accumulation of potassium
in the transverse tubular system, which then leads to persistent post excitation of
the membrane and continued contraction of the muscle (4,21,32,39,80,86,88,101).
Xanthosis. This condition occurs in cattle, without clinical signs, and is important
only in meat inspection. There is brownish discolouration of the muscle; cardiac,
masseter and diaphragmatic muscles are involved most frequently. Histologically
there is an accumulation of lipofuscin-like pigment close to the nuclear poles in the
muscle cells, in some cases mild myopathic changes are present (13,31).
Myopathy of the pectineus muscle in dogs. This condition is recognised in both
pure-bred German Shepherds and in mongrels. Usually bilateral in the pectineus
muscle, a retardation of the growth of type II muscle fibres, with compensatory
hypertrophy of type I fibres and predominance of type I fibres is present. However,
the disorder is mainly a developmental abnormality, and congenital absence cannot
be excluded. The morphological changes are typical for a primary defect in the
nervous system. Until now this has not been investigated, however. For that reason
this myopathy is provisionally classified as a primary myopathy. This condition
may play a part in the pathogenesis of hip dysplasia (19,49,88).
Myopathy of cachectic sheep. In muscles of sheep killed in the terminal stage of
wasting disease and without clinical evidence of neuromuscular disease, a trans-
formation of muscle cells from one type to another and a progressive atrophy of
type II cells can be found. There is reduction in the number of myofibrils and
striking loss of glycogen from the muscle cells. Degeneration and necrosis of muscle
cells is seen in only longstanding cases of starvation. Reduced caloric intake is
responsible for this phenomenon (48).

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